Factors affecting gas exchange by collateral ventilation in the dog

Respiration Physiology (1972) IS, 52-69;

FACTORS

AFFECTING

GAS EXCHANGE

VENTILATION

D. C. FLENLEY’, Department of Medicine,

Norih-Holland Publishing Company, Amsterdam

BY COLLATERAL

IN THE DOG’

L. WELCHEL

and P. T. MACKLEM

University of Edinburgh, Edinburgh, Scotlund and Respiratory Service, Royal

Victoria Hospital, and McGill University, Montreal, Canaak

Ah&r& We measured oxygen and carbon dioxide tensions in gas sampled from a catheter wedged into a small subsegmental airway of paralysed dogs during positive pressure ventilation. The wedged catheter obstructed this airway, so that the alveoli it served were then only ventilated through collateral channels from adjacent airways or airspaces. Oxygen tensions of these samples lay between the alveolar and arterial tensions, being well above the mixed venous levels, indicating that collateral channels could provide considerable ventilation to the alveoli with an obstructed airway. Increase in lung volume did not improve gas exchange in the collaterally ventilated alveoli, nor was this greatly impaired by rapid rates of ventilation. Collateral ventilation became more efficient as the ventilation perfusion ratio of the whole animal increased. Our results suggest that functional collateral channels in the dog are more likely to communicate between alveoli than between small airways. Collateral ventilation could be important in maintaining alveolar ventilation in patients with airway obstruction.

Airway occlusion Collateral ventilation

Pulmonary gas exchange Ventilation-perfusion ratio

Dog

Neither the mechanical properties nor the efficiency of gas exchange are grossly disturbed by experimental obstruction of some of the 2 mm diameter airways in lobes of the dog lung (Brown et al., 1969; Flenley et al., 1972). Collateral channels appear to communicate between either alveoli or distal small airways in this species, so allowing ventilation of those alveoli originally served by the airways which have been obstructed. We have measured the oxygen and CO, tensions in gas obtained from airspaces which are only supplied by such collateral channels, as we varied alveolar ventilation, lung volume and ventilation rate. We have tried to find if collateral channels are more likely to communicate between small airways than between alveoli in the dog lung. Accepted for publication 6 January 1972.

’ Supported by a grant from the Defense Research Board of Canada. ’ Reprint requests: D. C. Flenley, Department of Medicine, University of Edinburgh, Royal Infirmary, Edinburgh, Scotland. 52

GAS EXCHANGE

BY COLLATERAL

VENTILATION

53

M&bOdS We modified the method of Lindskog and Bradshaw (1934) to sample gas from collaterally ventilated spaces during positive pressure ventilation in 12 supine closed chest male dogs weighing 18.2-26.4 kg, anaesthetised with chloralose (66 mg/kg) and urethane (5.5 ml/kg), and paralysed with 2% succinyl choline. We placed catheters in the carotid and main pulmonary arteries, and passed a radio-opaque catheter (outside diameter 2.3 mm) through a tracheostomy to wedge firmly and so obstruct a small subsegmental lower lobe airway (figs. 1 and 2). An outer sliding sheath then tamped a putty-like substance, Duxseal, (Canadian Johns Manville Co.) to form a seal around the wedged catheter. Airway occlusion was shown by movement of the catheter with each breath, and by the distinct tug needed to remove a wedged catheter at the end of a study, when the overlying pleura, then exposed at post mortem, was seen to dimple (fig. 3). A Harvard respirator ventilated the dog with either air or 100’~ oxygen, tracheal Pcol being monitored by a Beckman LB-1 analyser. Expired gas passed to a mixing box, dry gas meter (Parkinson Cowan) and underwater seal to

>

Fig. 1. Method of sampling gas from that collaterally ventilated space (CVS), normally ventilated by the airway obstructed by the wedged catheter. The sliding sheath tamped Duxseal around this catheter to ensure obstruction, and gas was sampled during expiration into syringe-s of the Harvard pump, through the CO2 micro-catheter cell and Sanbom differential transducer, sampling pressure always being abqve ambient.

D. C. FLENLEY, L. WELCHEL AND P. T. MACKLEM

Fig. 2. In oioo lead dust bronchogram at the end of an experiment, with a 1 mm diameter probe (arrowed) passed through the 2.3 mm diameter wedged catheter into an airway of this CVS. These airways are not outlined by lead dust. The approximate size of this CVS is indicated by the dotted lines and the diaphragmatic lung border (solid line).

control pressure across the respiratory system (Prs). We continuously recorded mixed expired 0, (Beckman E2) and CO, concentrations (Godart Capnograph), expired and tidal volumes, and carotid, pulmonary arterial, and tracheal pressures.

GAS EXCHANGE

BY COLLATERAL

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55

Fig. 3. In uiuoview of the diaphragmatic pleural lung surface. In A the lung is deflated and the wedge catheter has been suddenly inflated, so outlining the pleural base of the CVS subtended by this 2.3 mm diameter catheter. In B the transpulmonary pressure is + 5cm H,O. In the original colour photograph there was no pallor of the pleural surface in B.

--WOLE Luffi

Fig. 4. Three compartment model of gas exchange in the lung and CVS. The minute volume of ventilation is Vtr, the ventilation of the alveolar component VP, the blood flow @, and that of the aiveoiar component @P. The superscript cvs ident~es these variables for the ~1lateraBy ventilated space. The model assumes equilibrium between alveolar gas and capillary blood.

A motor driven Harvard withdrawal pump, activated only during expiration, slowly sampled gas from the wedged catheter into paraffined glass syringes, with subsequent measurement of P,, (LB-i) and Po, (Beckman E2) in these mixed samples.

56

D. C. FLENLEY,

L. WELCHEL

AND

P. T. MACKLEM

We also collected carotid and mixed venous blood samples throughout these 10-20 min sampling periods, for measurement of P 02, PcoI, pH (I. L. Electrodes) and haematocrit. Minute ventilation and expired gas concentrations were constant before and during each period, so ensuring a steady state of gas exchange. The lungs were inflated to Prs + 30 cm water 5 min before each sampling period. Calculations The collaterally ventilated space (CVS) is that volume of lung normally ventilated by the airway obstructed by our wedged catheter. We describe gas exchange in both the whole lung and the CVS by the three compartment model described by Riley and Pet-mutt (1965) (fig. 4), and again use their symbols to define components of the mixed expired gas (VE) and pulmonary blood flows (Qa) (Flenley et al., 1972). Gas tensions in the alveoli of the CVS are thus ~cy8 and ToI”, where the superscript ac, cvs refers to the alveolar compartment of the mixed expired gas from the CVS. In this model any end capillary diffusion gradient is included in the shunt compartment, but as our dogs breathed either air or 100% oxygen such gradients are probably negligible. We define the gas tensions in samples drawn from our wedged catheter as equalling PE$‘“’ and PE?~?. Alveolar gas in this model is thus in equilibrium with the alveolar component of pulmonary blood flow, so that

where Paa’*‘“’is the tension in the alveolar component of blood which has perfused the CVS. The oxygen content of this blood is C~z~cvs (ml/100 ml). The ventilation to perfusion ratio of the alveolar component of the CVS is VnaC.CVS 8.63 (Caac*cvs- CP,,) *R, cvs Qanc.cvJ= Paac*cvJ co2 where CXo, is the oxygen content of mixed venous blood, and the gas exchange ratio R,

cvs =

Psi;vs- Pko, PIo2 - PE$C”S

where PI,, and PI,,, are the inspired tensions (using conventional Otis, 1964). By substitution,

nomenclature,

For the whole animal, we can calculate the ratio of the alveolar ventilation (VE”) 1) to the whole pulmonary blood flow (Qa): 8.63 (Ca,, - ccl,,). R Cao, being the oxygen content of arterial blood ; 2) to the alveolar component of the pulmonary blood flow (Qaac):

GAS EXCHANGE BY COLLATERAL V~NTI~TION

57

Here, Ca& the oxygen content of the alveolar c~m~nent of the pulmonary blood flow, is derived from the alveolar Po,(wJ, obtained by the alveolar air equation (Otis, 1964). Solutions to eqs. (l-3) were obtained from our measurements. Conventional equations (Otis, 1964) gave VE, \jo2, R, and cardiac output (Qa). We did not sample dead space gas in the unobstructed airways adjacent to our CVS. This gas could have been re-inhaled into the CVS during the next inspiration However, assuming that R, cvs =0.8, and Caoz - Goz =4.5 ml/100 ml, eq. (1) shows that would only fall from 0.50 to 0.48 if PI,--~ rose from 0 to 20 mm Hg from reinhalation of dead space gas, and from 2.00 to 1.90 for the same rise in PI coz at this higher ventilation perfusion ratio. Least squares regression equations involving ventilation perfusion ratios were made after logarithmic transformation, as the frequency distribution of our observed values approximated to a logarithmic rather than to a normal distribution (Snedecor and Cochran, 1967). ~,fC.C-/QaWS

When ventilated with air at 10-40 br~ths~~in with Prs of f&3 cm water, the 12 dogs had a mean oxygen consumption of 6.83 (SEM 0.21) ml srp/min/kg body wt, cardiac output 132 (SEM 8) ml/min/kg body wt, respiratory exchange ratio (R) 0.77 (SEM 0.02), Pao,, 75.0 (SEM 2.2) mm Hg, and mixed venous Po, (PcIo,) 41.1 (SEM 0.6) mm Hg. To find if sampling from the CVS arti~~ally increased collateral ventilation we compared the gas exchange of the CVS indicated in gas samples drawn at a low sampling rate (3.0-3.2 ml/min) and a higher sampling rate (5.3-6.0 ml/min) (a). We then compared gas exchange in the CVS and the whole animal as we changed (b) alveolar ventilation, (c) lung volume, and (d) ventilator rate. (a) R4TE OF SAMPLING FROM THE CVS

There was no significant difference in the gas tensions or ventilation perfusion ratio of the CVS (fig. 5), between 9 paired consecutive samples drawn at the high and low sampling rates in 4 dogs. Each pair of samples was obtained in the same dog, at the same ventilator rate, tidal volume, gas exchange and cardiac output. (3pCVS/QaaC.CV8

)

(b) GAS EXCHANGE IN THE CVS AND THE WHOLE ANIMAL

Figures 6 and 7 compare the Po, of gas from the CVS with the alveolar, arterial, and mixed venous Po, on 21 occasions in 10 dogs, when ventilated with air at Prs a.3 cm Hz0 and 12-30 br~ths/~. The Po, of the CVS (~,c;~“‘) correlated both with alveolar (P >O.OOl) and arterial (0.01 > P >O.OOl) Po,, but not with mixed venous levels. The Prz$cys rose from arterial towards alveolar levels as we improved oxyge-

58

D. C. FLENLEY. L. WELCHEL AND P. T. MACKLEM 4.0 3.5

3.0

2.5

2.0 I.5

I.0

0.5

0

0.5

I.0

I.5

2.0

2.5

3.0

3.5

4.0

Fig. 5. Ventilation perfusion ratios of the CVS (Ik’c~cv’/~a’c~cn)in 9 p airs of consecutive samples drawn at the high and low sampling rates in 4 separate dogs. The calculated regression (---) is not significantly distinguished from the line of identity(---).

nation by increasing the alveolar ventilation of the whole animal (fig. 7). There was no significant difference between the Pcol of the CVS and that of arterial blood in 35 simultaneously drawn samples in 12 dogs (fig. 8). We found the ventilation perfusion ratio of the CVS (VEPC~CY’/~a~C*CVs) to be highly correlated (PC 0.001) with the ratio of alveolar ventilation to total lung perfusion of the whole animal (VrY/Qa) in 27 comparisons, again when the dogs were ventilated with air at Prs O-3 cm water, and 12-30/min (fig. 9). The regression equation was

(4)

log (log)=

0.48log

~0~~)+0.50,(P<0.001).

There was a similar correlation between the VEBc~cYS/~aac~cvs and the ratio of alveolar ventilation to the alveolar components of pulmonary blood flow, of the whole animal (VEBc/QaPC),th’IS re gression cquation(fig. 10) being: log

i

10 $J

1

= 0.3410g j10~~)+0.76,(P<0.001).

The CVS had a lower ventilation to perfusion ratio (expressed in these terms) than that of the whole animal on all but 4 of 26 occasions. (c) LUNG VOLUME

The relationship between the ventilation perfusion ratio of the CVS (Vr?C*CYS/~aPc*CvS) and of the whole animal (Vt?/Qa), observed in 12 sampling periods in 8 dogs (ventilated with air at Prs O-l cm H,O), could not be distinguished from the same relation-

GAS EXCHANGE

20

BY COLLATERAL

Ko

3040Y)60x)Bo00

59

VENTILATION

II0

120

-

PEqcv3 mmHg 02 Fig. 6. Relationship between arterial (O--O), and mixed venous (a--O) PO,, and oxygen tension in the CVS (w;‘“‘) in 10 dogs, ventilated with air at Prs O-3 cm Hz0 and 12-30/min. The regression lines are PaQ = 34.5 +0.43 (&)y),

(0.01 > P >O.ool)

W,, = 49.7 +0.08 (F’E$~“‘),

(P >O.lO).

ship calculated from 4 periods in 2 other dogs, again when ventilated with air but at a higher Prs of 9-l 1 cm water (fig. 11). As the arterial and mixed venous gas tensions, tidal volume, and ventilator rate were similar at both levels of Prs, we conclude that gas exchange by collateral channels was not affected by this rise in end expiratory lung volume. (d) VENTILATOR

RATE

(f)

We compared the ventilation perfusion ratio of the CVS (V~c*cvs/~aac~cvs)with that of the whole animal (V?/Qa) in 25 periods in 5 dogs ventilated with air at Prs &l cm H,O, at either low (15_27/min), or high (61-70/min) ventilator rates. We found no significant difference in these relationships at the two rates (fig. 12). Discussion original airway to the CVS was obstructed by the wedged catheter, any ventilation to this space must pass through collateral channels, either from adjoining

As the

60

D. C. FLENLEY, L. WELCHEL AND P. T. MACKLEM

pE-ram 4

Hg

Fig. 7. Relationship between mixed venous (---), arterial (--), and alveolar PO, (p&J ( x -.- x ), and the oxygen tension in the CVS (PF$‘“) in the same 10 dogs as in fig. 6. The regression equation ~,:=47.2+0.54(~;c*‘),

(P
(x-.-x)

describes the relationship between PO1of alveolar gas and the CVS.

airways or ventilated alveoli. If our sampling rate from the CVS was excessive, thereby pulling air through collateral channels, we would then artificially increase 3EaC’C”/ Qaac*cv3* However, doubling our rate of, sampling had no consistent effect on either the gas tensions or on VrFcV~/~aPC*cV* (fig. 5) so we avoided this error. If a leak had occurred past the “Duxseal” occlusion, it would contribute to the “collateral ventilation” as measured in our studies. We presume that 2.3 diameter airways were filled with inspired gas at the end of inspiration, so that such a leak would lower the observed w:. This would move the relationship shown in fig. 8 away from the line of identity, whereas we could not distinguish statistically between the Pcol of CVS gas and of the arterial blood. Over 30 years ago, Lindskog and Bradshaw (1934) first demonstrated the remarkable efficiency of gas exchange by collateral channels in the dog lung. Our results confirm this. In 6 out of 9 of their experiments, the Pcol of their “CVS” was slightly lower than that of the simultaneously measured arterial blood. With modern techniques we were able to measure not only PCoI, where the arterio-venous difference of 2-7 mm Hg is close to the accuracy of the measurement, but also Po2, with arteriovenous ditferences between 15 and 45 mm Hg. The Po, of the CVS gas lay between the arterial PO1and the alveolar Po, (as calculated from the alveolar air equation),

GAS EXCHANGE

BY COLLATERAL

VENTILATION

61

AfWML

pco2

mm Hg

Fig. 8. Relationship between the P,, in arterial blood (Pa,,,) and in the CVS, (Gy) 10 dogs, under the same conditions as in fig. 6. The regression equation is W0,

=

11.86+0.71(~;“).

in 35 samples in

(0.01 >P>O.OOl).

and always above the mixed venous Po, (figs. 6 and 7). The CVS must thus have enjoyed a considerable ventilation through collateral channels, although this was less effective than normal ventilation by unobstructed airways, for fig. 10 shows that ~Eac.CV8JQa8c.CVI was nearly always less than the comparable expression for the ventilation perfusion ratio of the whole animal (\jEBC/QaaC, the alveolar ventilation divided by the alveolar component of pulmonary blood flow). Where are these collateral channels, and what facto:s influence the efficiency of ventilation through them? Their anatomy is not established. The obvious contender, the pores of Kohn, communicating between alveoli, may number between 10 and Xl per alveolus in the dog (Martin, 1963). However, if a pore became closed by a liquid meniscus, a large pressure difference would be necessary for it to reopen, because of the small radius of curvature (Martin, 1966). l!he canals of Lambert (1955), between alveolar ducts and respiratory bronchioles, have been little studied. Unless they are very compliant it seems unlikely that either these canals or the pores of Kohn are the only collaterals in the dog, for Martin (1966) has passed spheres of 120 p diameter through such collaterals. He has demonstrated communications from respiratory bronchioles to alveolar ducts in this species. Measurements of gas tensions in lobar pulmonary

62

D. C. FLENLEY, L. WELCHEL AND P. T. MACKLEM

Fig. 9. Relationship between the ventilation perfusion ratio of the whole animal (Ib?/Oa) and that of the on logarithmic scales, in 27 samples in 10 dogs under the same conditions as fig. 6. CVS (V~c*cv~/~a’c~cv*), The regression equation is : = 0.48 log(l0 Vk?f~c*‘/Qa~c*c*‘) + 0.50 .

log( 10 */aa)

venous blood after lobar small airway obstruction led us to conclude that collateral channels in the dog lung could communicate either between alveoli or small airways (Flenley et al., 1972). Our present studies of factors affecting collateral ventilation let us estimate which of these is most likely to be the major site of collateral channels in the dog. We start by defining the efficiency of collateral ventilation (E ~011)as the ratio of the tidal volume per unit volume of the CVS, to that of the whole lung VT cvs VL .x loo”/O

Ecoll = -

V CVS

VT

where VT cvs V = tidal volume of the CPS, V cvs = volume of the CVS at FRC, VL = FRC of the whole lung, VT = tidal volume of the whole lung. Ventilation per unit volume of the lung in our supine animals will be fairly uniform throughout (Faridy, Kidd and Milic-Emili, 1967) so that E co11can also be expressed

GAS EXCHANGE

BY COLLATERAL

VENTILATION

63

s29P" 4

Qc a

I.0-l 0.5 -

Fig. 10. Relationship between the ventilation perfusion ratio of the whole animal, expressed in terms of alveolar ventilation and the alveolar component of pulmonary blood flow (3ELC/Qa’C),and that of the CVS, on logarithmic scales, in 26 samples in 10 dogs under the same conditions as fig. 6. The regression equation is : log( 10 !W/Qa) = 0.34 log (10 3Pcv’/Qa’c*cva) +0.76 .

as the ratio of Vr cvs to the tidal volume of the potential CVS before obstruction of its airway. We can estimate E ~011,starting from the relationship that we observed experimentally when f = 12-30/min and Prs = O-3 cm Hz0 (fig. 9)

(4

log

(

10 g

>

= 0.48 log (lo~J+os.

As this regression coefficient, 0.48, does not differ statistically from 0.50, doubling both sides of this equation, and taking antilogarithms, reduces this equation to the parabolic form

In our three compartment (6) (7) (8)

model (fig. 4)

VE? =(l-D)VE VtiC’cVS= (l-d)vE

64

D. C. FLENLEY, L. WELCHEL AND P. T. MACKLEM

0.1

0.2

0.5

I.0

2

5

lo

\iE ac,cvs

L

aa ac,cvs

Fig. 11. Relationship between the ventilation perfusion ratio of the whole animal (Vt?/Qa) and that of the CVS, (V~c*c~/Qa’c~c*’ ) on logarithmic scales at Prs O-l cm H,O (a), and Prs 9-11 cm H,O (0). The regression equation (O--O) at Prs O-l cm H,O is: log(lOVE”/Qa) = 0.57 log(103t?~cv’/Qa”*c”) +0.41 (P r0.001) . The points at Prs 9-11 cm H,O (0) lie on the same regression line.

3~ =

f. VT = minute volume of the whole lung

D = $, d

where VD is the physiological dead space of the whole lung.

= VDCVS where VDCVSis the physiological VTCVS’ dead space of the CVS. Qashunt,

s

cvs

the venous admixture ratio of the CVS.

=QaCVS3

We assume that the blood flow per unit volume is tht? same for the whole lung and for the CVS, or : (9)

(10)

VL =K-Vcvs Qa = K . Qacvs

GAS EXCHANGE

Fig. 12. Relationship

BY COLLATERAL

between the ventilation

the CVS (3tiC*cv’/Qa U*c”‘)on logarithmic

VENTILATION

perfusion ratio of the whole animal (‘@@a)

scales at low (1627/min,

0) and high(61-70/min,

65

and that of 0) ventilator

rates. The regression equation (--) log 10 W/Qa

= @49 log 103~c~c*1/Qa~c*cv~+ 0.51 (P >O.OOl) describes the relationship

for all the points.

where K is a constant. This assumption seems justified, for in oivo occlusion of small airways of a dog lobe, leading to the creation of numerous collaterally ventilated spaces, did not change the total lobar blood flow (Flenley et al., 1972), and gravity would have minimal effects on distribution of blood flow or ventilation in our supine animals. By substitution from (6), (7), (8) and (10) into (5) we obtain : 3~“’ Qa’

f*V-r(l-D) = K.QaCVS

f-VT

CVS(1-d)

(1-s). Qacvs

and by substituting from (9) and cancelling :

(11)

\;rE” (1-D)( l-s)

*.

(lo)

VT cvs ==.

VL Vr

=

E ~011.

D. C. FLENLEY,

66

L. WELCHEL

AND

P. T. MACKLEM

Equation (11) shows that the efficiency of collateral ventilation (E ~011)is a linear function of the ventilation/perfusion ratio, and also of the dead space ratio of the whole animal, and of the venous admixture ratio of the CVS, but an inverse function of the dead space ratio of the CVS. Mechanical factors determining E co11are discussed by Macklem (1971) who shows that :

021

E co11 = i

1 + ~--(2rdlT. co11)2 + 60 /

where T co11 (the time constant for collateral ventilation) =RcD,, +C cvs. Rco,, is the resistance to collateral flow, and Ccvs is the effective compliance of the CVS, which in turn depends upon V,cvs and the degree of interdependence between the CVS and the rest of the lung (Ma~klem, 1971). Direct me~urements of T co11 in the dog gave values between 0.03 and 1.0 set at FRC (Woolcock and Macklem, 1971), T co11being usually less than 0.1 set at FRC when V cvs was below 50 ml. If T co11was 0.1 see, substitution in eq. (12) shows that E co11 would fall from 98% when f was 20/min, to only 81% when f rose to 70/min. By equating these two expressions for E co11 (eqs. (11) and (12)). we obtain: VEP‘. (LD)( l-s) (13)

pa

(1-a)

(2nf!T calf)’ i 60

which relates VrY/Qa to the dead space ratio of the CVS (d). Figure 13 shows this relationship when f was 2O~min and 7O/min, from our average measured values of D at these two ventilator rates, T co11 of 0.1 set (Woolcock and Macklem, 19711, and is assumed constant at 5 %. The dead space ratio of the CVS (d), falls as Vr?/Qa rises. By substitution from eq. (6) into eq. (13) we obtain : VT.f.(l-D)2*(l-s) (14)

T--d)

(2zf!T ~011)~ * 60

relating VT to d. Substitution of the same values as for fig. 13 with our average values of Qa observed when the dogs were ventilated at 16-27/min and 61-70/min, gives the relationship shown in fig. 14. The dead space of the CVS(d) falls as VT rises, but is always slightly greater at the lower ventilation rate, at the same tidal volume. Lung inflation did not affect CVS ventilation as the tidal volume of the lung did not change. These arguments depend on the validity of our gas exchange model, where we equate gas with blood tensions in our “ideal” alveolus, and use our wedge catheter samples to measure these “ideal” alveolar tensions. Can we justify these two claims? Arterial P,, could exceed Pn& by at most 3 mm Hg in the range of values of R(0.77 + SEM 0.02), Pa,,(25-70 mm Hg), and shunt (maximal 9%), which we encountered. This error could lead to errors in calculated Vr?/Qa and %?Yc/Qaacof up to 12oj,,

GAS EXCHANGE

BY COLLATERAL

VENTILATION

67

Fig. 13. Solutions to eq. (13) as described in text. !b’

(1-D)(l-s)

1 1 + (2nfT ~011)~’

Qa.x= 1

60

1

when f=20/min, D=33%, s=S’/& T coll=O.l set, and when f=70/min, D=64%, s=5% and Tcoll=O.l SK, d = VD CVS/vT CvS.

which would not seriously affect our conclusions. The constant composition of our wedge catheter samples, despite doubling the rate at which they were drawn, implies that they came from a homogeneous source, which is most likely to be the alveolar gas 3 the CVS, as our catheter sampled from the centre of the CVS, whereas collateral ventilation must enter by its periphery. Contamination of our samples with dead space gas is thus unlikely. We suggest that figs. 13 and 14, derived both from our results, observed values of T co11 (Woolcock and Macklem, 1971), and a reasonable assumption for the venous admixture ratio of the CVS, imply that much of the collateral ventilation in these dogs was passing between gas exchanging structures. By our definition the dead space of the CVS is that part of its ventilation which does not partake in gas exchange, so it includes gas which has already come into equilibrium with capillary blood in adjacent alveoli. The high values for dead space of the CVS (figs. 13 and 14) indicate that such gas constitutes a considerable portion of CVS ventilation. We feel that collateral ventilation between small airways can hardly account for such a large CVS dead space. The fall in dead space as both VP/Qa and VT are increased could arise from a more eflicient wash-out of such adjacent alveoli into the CVS. The slight reduction in dead space at the higher frequency might be the result of limitation of the

68

D. C. FLENLEY, L. WELCHEL AND P. T. MACKLEM

0

2%

SBr, VD,CVS vT,cvs

Fig. 14. Solutions to e-q.(14) as described in text VT.T.(I-D)~.(I-S) Qa(ld) with values as in fig. 13 including Qa = 3.0 litre/min, when f = 20 and 70/min.

time available for any gas exchange in these adjacent alveoli, so leaving more “fresh” gas available for ventilation of the CVS. These studies therefore suggest that collateral channels are most likely to communicate extensively between alveoli in the dog lung. Collateral channels are probably scarce in the normal human lung, yet may become important channels for ventilation in patients with obstructed airways (Hogg et al., 1969). If we can extrapolate to these human diseases from our studies in the dog, where collateral channels are functionally prominent, our results would suggest that a relatively high overall ventilation/perfusion ratio provides optimal collateral ventilation. The high ventilation/perfusion ratio in an attack of bronchial asthma or pulmonary oedema, as evidenced by the low Pa,, seen in these patients (Tai and Read, 1967 ; Iff and Flenley, 1971), might serve to optimise collateral ventilation when some small airways are severely narrowed or closed. Further studies in man appear warranted. References Brown, R., A. J. Woolcock, N. J. Vincent and P. T. Macklem (1969). Physiological eNects of experimental airway obstruction with beads. J. Appl. Physiol. 27: 328-335. Faridy, E. E., R. Kidd and J. Milic-Emili (1967). Topographical distribution of inspired gas in excised lobes of dogs. J. Appl. Physiol. 22, 760-766. Flenley, D. C., J. Picken, L. Whelchel, F. RUN, P. M. Corry and P. T. Macklem (1972). Blood gas transfer after small airway obstruction in the dog and minipig. Respir. Physiol. 15: 3%51.

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